The role of uric acid in the risk of hypertension developed from prehypertension: a five-year Chinese urban cohort study.

IF 3.2 3区 医学 Q2 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH
Jun Zhu, Lingyu Shen, Shifen Jia, Wei Wang, Yaqing Xiong
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引用次数: 0

Abstract

Background: Uric acid as a prominent causal factor in the pathogenesis of hypertension is well recognized. Nevertheless, the influence of uric acid on the transition from prehypertension to hypertension within the Chinese population remains understudied.

Methods: A cohort of 1,516 prehypertensive individuals, aged 35 to 84 years, underwent recruitment following a comprehensive health assessment in 2017 and subsequent re-evaluation in 2022. Baseline characteristics and relevant clinical data were collected. The analytical approach encompassed multiple logistic regression and propensity score matching.

Results: Over 5 years, the cumulative incidence of hypertension amounted to 35.1%, with 33.9% in males and 37.3% in females, respectively. Notably, prehypertensive subjects concomitant with hyperuricemia exhibited a higher cumulative incidence of hypertension in comparison to the non-hyperuricemic counterparts (40.7% vs. 34.0%, p = 0.041). Multiple logistic regression unveiled a significant association between hyperuricemia and heightened hypertension risk (adjusted odds ratio [OR] = 1.44; 95% confidence interval [CI], 1.05-1.98; p = 0.022). Nonetheless, this association did not reach statistical significance when examining female subjects (adjusted OR = 1.10; 95% CI, 0.58-2.09; p = 0.781) or participants aged ≥ 60 years (adjusted OR = 1.07; 95% CI, 0.61-1.88; p = 0.814). Further validation through propensity score matching affirmed that subjects afflicted by hyperuricemia experienced a substantially elevated risk of transitioning from prehypertension to hypertension over the course of five years compared with the non-hyperuricemic counterparts (41.3% vs. 32.3%, p = 0.045), after adjusting for 12 covariates including age and gender. Hyperuricemia emerged as an independent risk factor predisposing individuals to the development of hypertension from a prehypertensive state.

Conclusion: This observation prompted the formulation of a hypothesis suggesting that ameliorating elevated uric acid levels may potentially mitigate the progression from prehypertension to hypertension.

尿酸在高血压前期发展成高血压的风险中的作用:一项为期五年的中国城市队列研究。
背景:尿酸是高血压发病机制中的一个重要致病因素,这一点已得到广泛认可。然而,在中国人群中,尿酸对高血压前期向高血压转变的影响仍未得到充分研究:在 2017 年进行全面健康评估后,招募了 1516 名高血压前期人群,年龄在 35 至 84 岁之间,随后在 2022 年进行了再次评估。收集了基线特征和相关临床数据。分析方法包括多元逻辑回归和倾向得分匹配:5年间,高血压的累计发病率为35.1%,其中男性为33.9%,女性为37.3%。值得注意的是,与非高尿酸血症患者相比,高尿酸血症前期患者的高血压累积发病率更高(40.7% 对 34.0%,P = 0.041)。多元逻辑回归揭示了高尿酸血症与高血压风险增加之间的显著关联(调整后的几率比 [OR] = 1.44;95% 置信区间 [CI],1.05-1.98;P = 0.022)。然而,在研究女性受试者(调整后的 OR = 1.10;95% CI,0.58-2.09;p = 0.781)或年龄≥ 60 岁的参与者(调整后的 OR = 1.07;95% CI,0.61-1.88;p = 0.814)时,这种关联并没有达到统计学意义。通过倾向得分匹配进行的进一步验证证实,在对包括年龄和性别在内的 12 个协变量进行调整后,与未患高尿酸血症的受试者相比,患高尿酸血症的受试者在五年内从高血压前期转变为高血压的风险大大增加(41.3% vs. 32.3%,p = 0.045)。结论:高尿酸血症是导致高血压患者从高血压前期状态发展为高血压的一个独立风险因素:结论:这一观察结果促使我们提出了一个假设,即改善尿酸水平的升高有可能缓解从高血压前期发展为高血压的过程。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Archives of Public Health
Archives of Public Health Medicine-Public Health, Environmental and Occupational Health
CiteScore
4.80
自引率
3.00%
发文量
244
审稿时长
16 weeks
期刊介绍: rchives of Public Health is a broad scope public health journal, dedicated to publishing all sound science in the field of public health. The journal aims to better the understanding of the health of populations. The journal contributes to public health knowledge, enhances the interaction between research, policy and practice and stimulates public health monitoring and indicator development. The journal considers submissions on health outcomes and their determinants, with clear statements about the public health and policy implications. Archives of Public Health welcomes methodological papers (e.g., on study design and bias), papers on health services research, health economics, community interventions, and epidemiological studies dealing with international comparisons, the determinants of inequality in health, and the environmental, behavioural, social, demographic and occupational correlates of health and diseases.
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